A stenosis is a stricture of a canal or duct. In the context of the vascular system a stenosis is a narrowing of the lumen of a blood vessel. A stenosis can severely restrict blood flow and promote thrombosis which can lead to myocardial infarction or stroke, for example. A common type of primary stenosis is caused by a buildup of atherosclerotic plaque.
Several therapeutic methods have been developed to improve circulation and homeostasis in stenotic vessels including by-pass surgery and revascularization procedures. Revascularization procedures (e.g. balloon angioplasty, bare metal stents as well as drug eluting stents, atherectomy, rotary ablation (rotablation)) serve to improve blood flow by reducing or removing the stenosis. However, these procedures frequently injure the blood vessel. The biological response to the injury is a multifactorial fibro-proliferative process that is similar to wound healing, and includes the elaboration of growth factors from a variety of cell types, infiltration of leukocytes, migration and proliferation of smooth muscle cells, the production of extracellular matrix and tissue remodeling. The process can result in the formation of a thick neointima within the vessel wall which reduces the luminal area of the vessel (e.g. restenosis). Various levels of restenosis occur following about 20-50% of coronary angioplasty procedures.
Attempts have been made at reducing restenosis following vascular intervention procedures by, for example, placing endovascular stents at the location of the stenosis. At present, this treatment sometimes itself causes restenosis. Stents are typically implanted within a vessel in a contracted state and expanded when in place in the vessel in order to maintain integrity of the vessel and to allow fluid flow through the vessel. Typically, implantation of stents is accomplished by mounting the stent on the balloon portion of a catheter, positioning the stent in a vascular lumen, and expanding the stent to an expanded state by inflation of the balloon within the stent. The stent can then be left in place by deflating the balloon and removing the catheter. One problem with stenting according to this widely used procedure, however, is that as the stent expands, it engages relatively brittle plaque lining the arterial tissues surrounding the stent, not the arterial tissue itself. In doing so, the expanding stent cracks the plaque to produce debris. This debris, in an untended condition, then enters the blood stream and occasionally injures the patient further by causing a vessel blockage downstream. This debris release is exacerbated by the fact that conventional stent structure contains large gaps, enabling the debris to move freely into the bloodstream. This debris creating effect is especially problematic when stenting in the carotid arteries, where the downstream blood flow leads directly to the brain and debris can cause strokes. In coronary arteries, debris is particularly dangerous because it can lead to heart attacks.
Currently, protection against this debris is carried out during the stenting procedure by using a downstream embolic shower protection device. This sort of device acts as a filter which traps debris of a predetermined size from transiting through the cardiovascular system. There are a number of drawbacks with using these embolic shower protection devices as they exist currently. One drawback is that they often encompass using another device, in addition to the balloon catheter which must be inserted into the patient, adding time and potential danger to the procedure. Another drawback is that the protection device must be downstream of the stent location, therefore, some additional stretch of vasculature must be available in order to properly position the protection device. Yet another drawback is that the embolic shower protection device is removed at the conclusion of the stenting procedure and therefore does not provide any protection after that point, despite the fact that post procedure debris can become potentially dislodged as a result of the procedure. Yet another drawback is that the embolic shower protection device is placed some distance from the stent, thus possibly leaving some close side branches unprotected.
Another common practice in use with stenting procedures is the use of stents for administering pharmacologic agents to treat restenosis and other body ailments through the lumen walk. Because of the mechanical strength that is required to properly support vessel walls, stents are typically constructed of metallic struts. However, these struts are often constructed to be thin because, in general, foreign material in the body is to be avoided and because of the need to obtain a stent that can be crimped, flexible and conform with the blood vessel anatomy. Arterial stents are built to cover a minimum amount of the blood vessel's walls, while still having a high radial force in order to avoid collapsing and thus keeping the lumen open. Typically, the metal struts cover only about 10% of the total covered area, and the stent somewhat resembles a cylindrical fishing net. However, one-drawback with these stents is that pharmaceuticals are placed only on the stent struts, which cover only a small portion of the blood vessel's wall, and they do not cover the apertures in the stent. Thus the therapeutic effects of the drug are achieved only on a small portion of the injured tissue. Since some pharmaceuticals are comprised of large molecules, with a very high molecular weight, and/or complicated and/or wide stereochemistry, and which have limited diffusion capabilities, there is a large area of tissue which is not effectively treated. Another drawback of current drug eluting stents is that in attempts to overcome the diffusion issues, an excessive amount of drug must be eluted in the hopes that it will permeate to the target tissue. In some cases, this causes undesirable overdosing of the tissue areas closest to the stem struts in addition to the added expense of using copious amounts of the drug. Furthermore, there are design limits which prevent increasing the amount of drug embedded and thus, eluted from the stent.
U.S. Patent Publication No. 2004/0030377 to Dubson et al., the contents of which are herein incorporated by reference, describes a stent assembly which is designed to deliver pharmaceuticals to a blood vessel after implantation while encouraging endothelial growth.
Today's drug eluting stents suffer from higher incidences of sub-acute thrombosis than the previous generations of bare metal stents. Longer administration period of anticoagulant drugs like Plavix® is needed, with additional cost and more side effects for the patients. The main reason for the sub-acute and the chronic thrombosis is sudden exposure of a small area of the stent strut to the blood stream. The small area of exposed stent typically happens when several adjacent endothelial cells fall from the stent strut surface leaving an exposed area of the strut structure and producing a site on which blood platelets can clot. Even if the patient is being treated with anticoagulants, there is a very high risk that the platelets will stick to the exposed stent and cause clotting. This phenomenon may lead to a total occlusion of the blood vessel and to an immediate myocardial infarction. Drug eluting stents are more susceptible to such incidences since the conformity and the integrity of the endothelial cells covering the polymer is not as good as when they are covering a bare metal stent.